Control mice adhered to endothelial cells from infected mice in a similar way that was observed in the infected group, confirming that schistosomiasis alters endothelial cell function. Endothelial cells are a major determinant of leukocyte adhesion and vascular permeability, and under normal conditions, they provide a well-known anti-inflammatory state. To achieve these functions, gene Navitoclax Bcl-2 inhibitor expression patterns are tightly regulated in endothelial cells. In this regard, eNOS expression plays an important role. For instance, in eNOS-null mice, but not in inducible NOS-null mice, there is a significant increase in the number of rolling leukocytes and vascular permeability suggestive of an up-regulation of inflammatory reaction in conditions of reduced eNOS-derived NO. In support to this idea, inhibition of eNOS increases leukocyte adhesion and migration in the murine peritoneal cavity, leukocyte adhesion to mesenteric vascular endothelium and vascular permeability. Therefore, we might suppose that eNOS-derived NO suppress endothelial cell activation in an autocrine fashion counteracting signals that mediate their activation. For instance, NO inhibits the endothelial expression of adhesion molecules such as intercellular adhesion molecule -1, which is essential for endothelial cell-leukocyte interaction. In this context, in schistosomiasis, there is an increase in the expression of ICAM-1 and plasma soluble ICAM-1, a marker of inflammatory diseases and endothelial activation. Vascular endothelial cells are the primary eNOS-expressing cell type being eNOS mRNA constitutively expressed. Steady-state eNOS mRNA levels are regulated at epigenetic, transcriptional and post-transcriptional levels. The knowledge about the mechanism and role of epigenetic regulation of eNOS expression continues to mount. In addition, the enzymatic activity is subject to post-translational regulation through protein-protein interactions. One such negative regulator is caveolin-1. Previous indirect data suggested a reduced production of NO in mice portal vein, but considering the phenotypic heterogeneity of endothelial cells, it was necessary to investigate NO production and eNOS expression in the present model. In fact, an impairment of ATP-induced NO production in cultured endothelial cells from infected animals was found in the present work, whereas NO production in the control group was similar to the level previously reported in similar experimental conditions. As a similar result was observed with A23187, which activates eNOS in a receptor-independent manner.